Excessive production of Immunoglobulin E (IgE) is the hallmark of allergic response to allergens. IgE exerts its primary role through cross-linking of the high-affinity IgE receptor (FcεRI) on mast cells and basophils, resulting in degranulation with the release of histamines and other molecules that produce symptoms associated with allergy.
In contrast, another membrane protein on B lymphocytes (also expressed on macrophages and platelets), CD23 (Fc68 RII), the low-affinity receptor for IgE, plays an important role in decreasing IgE-associated allergic response through regulation of IgE production.
Therefore, therapeutic substances that inhibit binding of free IgE to high affinity receptors on mast cells and basophils can be useful to reduce allergic symptoms. It would also be advantageous if such substances also did not substantially interfere with IgE binding to the low affinity receptors on B lymphocytes so as not to increase IgE production.